scholarly journals erbBGenes in the Mouse Uterus: Cell-Specific Signaling by Epidermal Growth Factor (EGF) Family of Growth Factors during Implantation

1998 ◽  
Vol 204 (1) ◽  
pp. 97-110 ◽  
Author(s):  
Hyunjung Lim ◽  
Sanjoy K. Das ◽  
Sudhansu K. Dey
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Mouse Uterus ◽  
Epidermal Growth ◽  
Egf Family

174. THE EPIDERMAL GROWTH FACTOR (EGF) FAMILY IN THE ENDOMETRIUM AND BLASTOCYST OF THE TAMMAR WALLABY, MACROPUS EUGENII DURING EMBRYONIC DIAPAUSE

2009 ◽  
Vol 21 (9) ◽  
pp. 92
Author(s):  
J. C. Fenelon ◽  
G. Shaw ◽  
M. B. Renfree
Keyword(s):  
Growth Factors ◽  
Cell Division ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Tammar Wallaby ◽  
Leukaemia Inhibitory Factor ◽  
Embryonic Diapause ◽  
Macropus Eugenii ◽  
Epidermal Growth ◽  
Egf Family

Embryonic diapause, a suspension of cell division and growth at the blastocyst stage, is widespread amongst mammals, but is especially common in the kangaroos and wallabies. In the tammar, Macropus eugenii, the sequence of endocrine events leading to embryonic diapause and reactivation are well defined[1]. The blastocyst can remain in diapause for up to 11 months without cell division, measurable metabolism or apoptosis occurring [2]. The ovarian hormones, especially progesterone, exert their effects on the blastocyst by alterations in the endometrial secretions [3], but the molecular cross-talk between the endometrium and blastocyst is unknown. There is increasing evidence for the involvement of leukaemia inhibitory factor (LIF)but the epidermal growth factor (EGF) family of growth factors are also likely to be involved.This study examined the expression of EGF and HB-EGF as well as their receptors, ERBB1 and ERBB4, in the tammar endometrium and blastocyst at entry into, and reactivation from, diapause. The genes for these factors were highly conserved in the tammar with orthologues in human and mouse. Quantitative RT-PCR of all four factors in the endometrium showed that expression changed with stage. Although expression levels of both receptors did not change between diapause and reactivation, both HB-EGF and EGF levels increased at reactivation from diapause and levels of HB-EGF decreased at entry into diapause. All factors were immunopositive in the endometrium. Studies underway will determine whether the cellular location and quantity of these factors change with entry into or exit from diapause, and define the molecular interactions occurring between the blastocyst and endometrium. These results are consistent with a role for the EGF family of growth factors in the control of embryonic diapause in tammars.

scholarly journals Estrogen Negatively Regulates Epidermal Growth Factor (EGF)-Mediated Signal Transducer and Activator of Transcription 5 Signaling in Human EGF Family Receptor-Overexpressing Breast Cancer Cells

2005 ◽  
Vol 19 (11) ◽  
pp. 2660-2670 ◽  
Author(s):  
Julie L. Boerner ◽  
Matthew A. Gibson ◽  
Emily M. Fox ◽  
Erika D. Posner ◽  
Sarah J. Parsons ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Egf Receptor ◽  
Signal Transducer ◽  
Epidermal Growth ◽  
Egf Family

Abstract Breast cancer cell growth may be stimulated by 17β-estradiol (E2) or growth factors like epidermal growth factor (EGF). However, tumors typically depend on only one of these pathways and may overexpress either estrogen receptor (ER) or EGF receptor (EGFR) and related family members. Tumors overexpressing EGFR are more aggressive than those expressing ER. Intracellular mediators of these growth-stimulatory pathways are not completely defined, but one potential common mediator of EGF and E2 signaling is the transcription factor signal transducer and activator of transcription 5 (STAT5). To investigate the role of STAT5 in potential crosstalk between E2 and EGF, MDA-MB231 and SKBr3 breast cancer cells, which are ER-negative and overexpress human EGF family receptors, were used. Introduction of ERα and treatment with E2 decreased EGF-induced tyrosine phosphorylation of STAT5b, basal and EGF-induced STAT5-mediated transcription, and EGF-stimulated DNA synthesis in these cells. Suppressive effects of E2-ΕRα were specific for STAT5, as EGF stimulation of MAPK was unaffected. Deletion/mutation analysis of ERα demonstrated that the DNA-binding domain was insufficient, and that the ligand-binding domain was required for these responses. ERα transcriptional activity was not necessary for suppression of STAT5 activity. Overexpression of c-Src did not prevent suppression of STAT5 activity by E2 and ERα. However, ERα did prevent basal increases in STAT5 activity with overexpressed c-Src. In the context of human EGF receptor family overexpression, E2-ER opposes EGF signaling by regulating STAT5 activity. STAT5 may be a crucial point of signaling for both E2 and growth factors in breast cancer cells, allowing targeted therapy for many types of breast tumors.

Insulin and epidermal growth factor are growth factors for isolated porcine thyroid follicles

1985 ◽  
Vol 110 (1_Suppla) ◽  
pp. S74
Author(s):  
R. GÄRTNER ◽  
W. GREIL ◽  
R. DEMHARTER ◽  
K. HORN
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epidermal Growth

Transforming Growth Factor α and Epidermal Growth Factor Receptor in Reactive and Malignant Mesothelial Proliferations

2004 ◽  
Vol 128 (1) ◽  
pp. 68-70
Author(s):  
Yun-Cai Cai ◽  
Victor Roggli ◽  
Eugene Mark ◽  
Philip T. Cagle ◽  
Armando E. Fraire
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Transforming Growth Factor ◽  
Malignant Tumors ◽  
Growth Factor Receptor ◽  
Transforming Growth Factor Α ◽  
Epidermal Growth ◽  
Factor Α

Abstract Background.—Growth factors such as transforming growth factor α (TGF-α) and epidermal growth factor receptor (EGFR) play an important role in cell proliferation. The immunohistochemical expression of these factors has been extensively studied in malignant tumors including mesothelioma. However, the comparative expression of these growth factors in mesothelioma and reactive mesothelial proliferations has been less well studied. Objective.—To evaluate the possible role of TGF-α and EGFR in the clinically important distinction between reactive mesothelial proliferations and malignant mesothelioma. Methods.—The expression of TGF-α and EGFR was studied in 39 cases of mesothelioma and 30 cases of reactive mesothelial proliferations by means of immunohistochemistry. Results.—Fourteen (70%) of 20 reactive mesothelial proliferations tested and 29 (76%) of 38 mesotheliomas tested expressed TGF-α. One (3%) of 30 reactive mesothelial proliferations and 17 (45%) of 39 mesotheliomas expressed EGFR. Conclusions.—These results suggest an up-regulation of EGFR in mesothelioma as compared with reactive mesothelial proliferations. This up-regulation further suggests a possible use of EGFR as an adjunct immunohistochemical test in the differential diagnosis of mesothelioma and reactive mesothelial proliferations.

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